Diseases caused by HTLV-1 have their etiologies in the dysregulated proliferation of human T-cells. This process has been attributed to the activities of the HTLV-1 transcriptional activator, tax. Recent data indicate that intracellular expression of tax results in constitutive NF-kB activation. Two mutants of tax, tax-N81 and tax-N109, which are deleted for amino terminal regions that are responsible for CREB binding and nuclear transport become localized to the cytoplasm. Although these mutants are unable to transactivate via HTLV-1 21 base pair repeats or by the serum response element, they continue to activate NF-kB at levels approximating or exceeding wildtype tax. Tax-N109 when transduced into primary lymphocytes using retroviral vectors, causes these cells to immortalize and undergo proliferation and apoptosis concomitantly. To explore immortalizing and transforming the functions of the tax-N mutants, the investigators will: Characterize of biological properties of the tax-N genes define interactions between tax mutants and components of the NF-kB signaling pathway determine biological and pathological effects of constitutive NF-kB activation by targeted tax-N mutant expression.